Feeding is largely guided by the sense of taste. it is now established that this influence is reciprocal: taste sensitivity is, to some degree dependent upon what has been eaten. This conclusion rests on the recognition of three emerging facts: (1) Taste-evoked activity is primarily devoted to encoding stimulus nutrition vs toxicity, a measure which parallels acceptance vs rejection behavior in rats and positive vs negative appreciation in humans. Thus, taste input carries information on the physiological value of a potential food, and it is on the basis of this information that feeding and the pleasure derived from it are determined. (2) Taste-evoked activity, in turn, is subject to modification according to the past experience or the momentary physiological needs of the organism. Thus, biochemical needs can influence the very taste input which guides feeding. The reciprocal interaction between taste and physiological condition presents a likely neural mechanism for the notion of body widsom. (3) This interaction takes place largely at the hindbrain level. The anatomical convergence through which such an interplay could function occurs in the hindbrain. Organisms with only the caudal brainstem intact respond appropriately to the nutritional vs toxicity dimension of taste, and change that reaction to meet many of the transient needs of the body. Several endogenous chemicals which affect feeding behavior have recently been identified. There is a widespread recognition that sensory influences, particularly those of taste, may be involved in mediating their actions. The aim of this proposed series of studies is to test that assumption directly. Taste-evoked responses will be recorded from single cells in the rat nucleus tractus solitarius before and after intravenous administration of each of six chemical factors which have been shown to influence feeding. If no changes in gustatory responsiveness occur with the manipulation, taste will be eliminated as a possible mechanism through which these substances might alter intake. More likely, taste activity will be affected. Such a finding would bear on two issues: (1) It would provide a specific mechanism through which the administered satiety factor might work and also strengthen the general notion of sensory-ingestive integration in the hindbrain. (2) It would address controversies of neural coding in taste, particularly the existence of gustatory neuron types.